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APOBEC3G targets human T-cell leukemia virus type 1
Amane Sasada1, Akifumi Takaori-Kondo, Kotaro Shirakawa
1Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaracho, Sakyo-ku, Kyoto 606-8507, Japan. amasasa@kuhp.kyoto-u.ac.jp
Retrovirology
|June 10, 2005
Summary
Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) inhibits human T-cell leukemia virus type 1 (HTLV-1) infection by incorporating into virions. This antiviral activity occurs independently of its cytidine deaminase function, suggesting unique mechanisms against HTLV-1.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) is a host protein with broad antiviral properties.
- APOBEC3G inhibits retroviral replication by inducing G-to-A hypermutation via deoxycytidine deamination.
Purpose of the Study:
- To investigate the antiviral activity and mechanism of APOBEC3G against human T-cell leukemia virus type 1 (HTLV-1).
Main Methods:
- Examined APOBEC3G incorporation into HTLV-1 virions.
- Assessed the antiviral activity of wild-type and mutant APOBEC3G against HTLV-1.
- Utilized HIV-1 vif gene to antagonize APOBEC3G in HTLV-1 producing cells.
Main Results:
- APOBEC3G, both overexpressed and endogenous, was incorporated into HTLV-1 virions, inhibiting infection.
- Inactive APOBEC3G mutants also inhibited HTLV-1, and no G-to-A hypermutation was observed in the HTLV-1 genome.
- Antagonizing APOBEC3G with HIV-1 vif increased HTLV-1 infectivity.
Conclusions:
- APOBEC3G inhibits HTLV-1 infection through virion incorporation, independent of its cytidine deaminase activity.
- The mechanism of APOBEC3G action against HTLV-1 differs from its action against HIV-1.
- APOBEC3G likely plays a role in the unique characteristics of HTLV-1 infection and transmission.